When a doctor declares a person dead, some of their body may still be alive and kicking – at least for a day or two. New evidence in animals suggests that many genes go on working for up to 48 hours after the lights have gone out.

This hustle and bustle has been seen in mice and zebrafish, but there are hints that genes are also active for some time in deceased humans. This discovery could have implications for the safety of organ transplants as well as help pathologists pinpoint a time of death more precisely, perhaps to within minutes of the event.

and at the University of Washington, Seattle, and their colleagues investigated the activity of genes in the organs of mice and zebrafish immediately after death. They did this by measuring the amount of messenger RNA present. An increase in this mRNA – which genes use to tell cells to make products such as proteins – indicates that genes are more active.

Noble’s team measured mRNA levels in zebrafish, and in brain and liver samples from mice at regular intervals for up to four days after death. They then compared these with mRNA levels measured at the time of death.

“Hundreds of genes with different functions woke up after death, including fetal development genes”

As you might expect, overall mRNA levels decreased over time. However, mRNA associated with 548 zebrafish genes and 515 mouse genes saw one or more peaks of activity after death. This meant there was sufficient energy and cellular function for some genes to be switched on and stay active long after the animal died.

These genes cycled through peaks and dips in activity in a “non-winding down” manner, unlike the chaotic behaviour of the rest of the decaying DNA, says Noble.

Hundreds of genes with different functions “woke up” immediately after death. These included fetal development genes that usually turn off after birth, as well as genes that have previously been associated with cancer. Their activity peaked about 24 hours after death.

A similar process might occur in humans. Previous studies have shown that various genes, including those involved in contracting heart muscle and wound healing, in humans who had died from multiple trauma, heart attack or suffocation (Forensic Science International, doi.org/bj63).

The fact that some genes associated with cancer are activated after death in animals, might be relevant for reducing the incidence of cancer in people who receive organ transplants, says Noble. People who get a new liver, for example, have more cancers after the treatment than you would expect if they hadn’t had a transplant. The regime of drugs they need to take for life to suppress their immune system so it doesn’t attack the new organ may contribute to this, but Noble says it is worth investigating if activated cancer genes in the donor liver could play a part.

So why do so many genes wake up after death? It is possible that many of the genes become active as part of physiological processes that aid healing or resuscitation after severe injury. For example, after death, some cells might have enough energy to kick-start genes involved in the inflammation process to protect against damage – just as they would if the body were alive.

Alternatively, a rapid decay of genes that normally suppress other genes – such as those involved in embryological development – might allow the usually quiet genes to become active for a short period of time.

For forensic scientists, knowing how gene activity rises and falls at different time points after death is useful for working out when someone died. Measuring mRNA would allow us to nail down the time since death to hours and possibly even minutes, rather than days, helping to reconstruct events surrounding the death.

It is good to see such progress being made in this area, says Graham Williams, consultant forensic geneticist at the University of Huddersfield, UK. “But substantial work is required before this could be applied to case work.”

The research also raises important questions about our definition of death – normally accepted as the cessation of a heartbeat, brain activity and breathing. If genes can be active up to 48 hours after death, is the person technically still alive at that point? “Clearly, studying death will provide new information on the biology of life,” says Noble.

Journal references: BioRxiv, ;

This article appeared in print under the headline “Genes get active after death”

You may forget your toothbrush next time you go away but you can’t leave your microbes behind. Millions of bacteria hitch a ride with you, making themselves comfortable wherever you go. Within only a few hours, they will have colonised a hotel room; give them 24 hours and they can take over an entire house.

These are just some of the results from the , the first attempt to trace the path of microbes from our bodies to our built surroundings, and vice versa. “We know that some microbes can increase our weight, we know that some can influence our neurological development, we want to know where those bacteria come from,” says from the University of Chicago, who leads the work.

The cells of our bodies are outnumbered 10 to 1 by the microbial cells that call our bodies home. Every time we breathe, sneeze or cough we leave traces of these microbial hangers-on. Others are left behind as we shed skin cells or touch surfaces. Given how much time we spend there, most of this microbial shedding is done at home. Despite this, we know surprisingly little about the interaction between our bodily microbes and those in our houses.

Microbial censor

To shed some light, Gilbert and his colleagues mapped the microbial signatures of seven human families, including three that were in the process of moving house. The families came from different parts of the US and were from different socioeconomic backgrounds and ethnicities. Over a period six weeks, the team took repeated swabs of the 18 family members’ feet, hands and nose. They also took samples from door knobs, floors, light switches and kitchen counter surfaces, as well as from any pets.

By amplifying and sequencing the genetic material in these swabs, the team isolated more than 21,000 different microbial species. Each family had its own distinct microbial signature that could be used to identify them. This signature was quickly transferred to the family’s living space, overwhelming the microbes already there. For example, one of the families moving house temporarily stayed in a hotel room. According to Gilbert, it took just 3 hours for their microbial signature to swamp the room, and less than 24 hours after they moved in to their new house for it to resemble their old one microbially.

Unsurprisingly, microbes transfer most commonly between hands and doorknobs, light switches and kitchen counters, and between floors and feet. Floor samples differed most between families. The smallest microbial variation between people was found between those in regular close contact, like couples, or parents and young children. There was greater variation between separate adults, for example, unrelated flat mates, and teenagers and their parents.

Young children, or people whose gut microbiota have been compromised by antibiotic use, for example, readily “accept” the microbes of others. Household pets were particularly good microbe “donors” – which persuaded Gilbert and his wife to buy a dog to increase the exposure of their family to a greater diversity of microbes, because this has been shown to reduce vulnerability to allergies.

The bugs are watching you

Gilbert says the research could be used to chart people’s movement around a house, and monitor their interactions. “We could tell how many individuals live there, and the relationship between them,” he says.

He recounts one case where a couple shared their home with a male lodger. Through analysis of the microbial samples from different parts of the house, the researchers could tell that the two men shared a bathroom, but the woman used another – a fact confirmed later by the couple. Theoretically, Gilbert says, analysis of microbial swabs could be used to detect a new relationship or uncover a cheating partner. If a database of people’s microbial profiles was ever created, a microbial signature or “fingerprint” could perhaps be used to identify criminals.

In the shorter term, such work could be used to recognise the presence of burglars in the house from an influx of unfamiliar microbes, or recognise alien microbes left on the skin of a homicide victim by the perpetrator – something that Gilbert is now working on in collaboration with the police department of Hawaii.

Journal reference: Science, DOI:

MILLIONS want you dead. No, it’s not a Twitter conspiracy, but a battle raging beneath your skin. The cells in your body are outnumbered 10 to one by microbial cells, and like it or not, eventually the microbes will win.

Surprisingly, what happens next has largely been a mystery. Now researchers have made the first study of the thanatomicrobiome – the army of gut microbes that take over your internal organs once you are dead. The results could have applications in forensic science and medicine.

While we are alive, the 100 trillion bacteria resident in our gut work on our behalf. They ease digestion and keep the immune system functioning smoothly, in exchange for a constant supply of food. These “friendly” bacteria adhere to the lining of the gut and keep the microbial villains at bay by outcompeting them.

After we die, however, our gut flora have a party. Dying cells leak carbohydrates, amino acids and lipids, causing a frenzy of microbial feeding and reproduction. The bacteria eventually escape the gut and swarm through the circulatory and lymph systems, spreading to organs that are shielded during life by the immune system.

“After we die, the bacteria in our gut swarm through our body to colonise our internal organs”

Understanding how microbes inside a dead body colonise it can help pathologists work out the time of death, where the body has been lying, and how its decomposition could affect the soil and ecology around it. Until now, research in this area has largely focused on the way that insects and microbes from a corpse’s environment take up residence in putrefying flesh.

To study how a dead body decays in isolation, at Alabama State University in Montgomery sampled microbes from a selection of internal organs, as “these aren’t influenced by environmental conditions”, he says. He hoped to discover how long it took gut bacteria to reach each organ after death, and establish which species go where.

Microbial signature

Traditional techniques for identifying microbes rely on growing them in Petri dishes, but gut bacteria are particularly tricky to culture. Instead, the team isolated and amplified bacterial genetic material from cadaver tissues to reveal the microbes present. Their samples came from the liver, spleen, brain and heart of 11 cadavers, between 20 and 240 hours after death.

In the newest cadavers, the researchers found bacteria such as Streptococcus, Lactobacillus and Escherichia coli, which mop up any oxygen left in the tissues after respiration stops. These gut flora are the “usual suspects” you would expect to find in most people.

As the time since death increased, the bacteria present were more likely to be those that can function without oxygen, such as Clostridium strains. For example, some of the cadavers harboured C. botulinum, which can cause botulism, and C. difficile, one of the main culprits in hospital infections. A more unusual strain, C. novyi, turned up in one body (see “Gut bugs united“).

Contrary to the team’s expectations, there was no predictable pattern of microbe distribution. This was a surprise, says Noble, as he had expected different microbes to thrive in different organs. For example, the team had thought that bile-tolerant species would flourish in the liver, whereas those adapted to iron-rich environments would do better in the spleen.

In fact, there was more variation between individuals and according to time since death than there was between the organs within a single cadaver (Journal of Microbiological Methods, ).

So does this individual variation mean that we can use the gut flora “signature” of a dead body to identify unknown victims of crime or a disaster, by matching it to bacteria on the unwashed clothes of missing persons?

“The only way to answer this is with a really big sample of cadavers,” says of the Sam Houston State University in Huntsville, Texas, who is . She points out that someone’s immediate environment is bound to have a strong influence on the microbes living in and on them, and therefore on their thanatomicrobiome. This means that even though an individual’s gut flora might be unique to them, they could also be broadly similar to those of people around them, making it hard to identify a person using bacterial profiling.

Even if it turns out to be impractical as a method of identification, there are other potential uses. Sequencing the DNA present could confirm a suspected bacterial infection, identify an infection when the cause of death was unknown, or even help assess the efficacy of antibiotics in treating an infection, says John Cassella, a professor of forensic science at Staffordshire University, UK.

What’s more, “the predictable shift in microbial colonisation of a body means we can use microbes as a clock to estimate how long a body has been decomposing”, says Bucheli.

“The predictable shift in microbial colonisation of a body means we can use it to estimate time of death”

Examining the internal organs could also be useful for bodies where the presence of microbial contamination on skin could confuse the investigation, says Cassella. He thinks it could help determine whether a body had been moved after death. For example, if someone died at home but their body was subsequently dumped elsewhere, the bacteria in their internal organs should have more in common with their home environment than where they ended up.

However it ends up being used, “cataloguing this ecosystem can help us understand how we coexist with microbial communities all around us”, says Bucheli. “The microbiome of a cadaver is an unknown data set in biology,” she says.

We may not have long to wait to find out whether the microbiome of death holds more surprises: Noble and his colleagues are about to start a bigger investigation, exploring the thanatomicrobiomes of 100 cadavers.

This article appeared in print under the headline “Death: the great bacterial takeover”

A third autopsy was conducted on Monday on the body of Michael Brown, the black teenager shot by a police officer on 9 August in Ferguson, Missouri.

Violent clashes have broken out between police and Ferguson residents over the killing, with witnesses and police putting forward different versions of what happened.

Did Brown have his arms up when he was shot? Was he ? The third autopsy, ordered by federal authorities, may not clarify what happened. “It is unlikely to be necessary,” says Michael Graham, a forensic pathologist at St Louis University, and will not find anything significantly different from the original one performed on the day Brown died.

The first autopsy, conducted by St Louis County Medical Examiner Mary Case, confirmed police accounts – that the 18-year-old was killed by gunshot wounds – though the number of shots that hit Brown was not made public.

Full details of the first autopsy are still under wraps. Brown’s family requested their own autopsy, which was performed by veteran medical examiner Michael Baden.

Baden, former chief medical examiner for New York, testified in the O.J. Simpson case, and chaired the panel reinvestigating the assassination of President John F. Kennedy. He has conducted some 20,000 autopsies.

His shows nine gunshot wounds: four on the right arm, three on the head and two on the chest – with no wounds on the back.

This appears to support the claim of the police officer who shot Brown, Darren Wilson, who says Brown was facing him when he fired. But other interpretations have been put forward. Dorian Johnson, a friend of Brown’s who was with him at the time, describes him being shot in the back.

In a press briefing after the autopsy, Baden said he needed more forensic evidence. “From a science point of view, we can’t determine which witnesses’ statements are consistent with the findings,” he said.

“Given this wound pattern, you could come up with a thousand positions and scenarios,” Graham says.

Baden states that Brown was shot at least six times, and the last bullet entered the top of his bowed head, killing him instantly.

But only three bullets were found in the body. The third autopsy, requested by federal authorities, may not be able to resolve the questions, since damage caused by the first and second autopsy may mean the third is compromised.

Several pathologists have aired their scepticism at Baden’s preliminary results. “It may be possible to account for these wounds with only three bullets, and not six as suggested,” says UK Home Office forensic pathologist Ben Swift, although he stresses that he was only working from images made public by Baden.

Another complicating factor is embalming. Brown’s body was embalmed after the first autopsy, which may limit the information discernable from the gunshot wounds, as the colour and texture of the body is altered.

Journal reference:

(Image: Stuart Palley/EPA/Corbis)

IT WAS raining fire and brimstone at Yosemite National Park, California. This long-exposure photograph taken in July on the park’s western border offers an ethereal, otherworldly view of the massive El Portal forest fire. Named after the gateway to the park, the fire, , at one stage covered around 14 square kilometres and . Summer is always fire season in the western states, but this year the battle against the blaze was exacerbated by .

Between 14 and 24 July, the National Park Service reported more than 3000 lightning strikes and so far this year, fire crews have had to fight more than 30,000 minor fires across several states, in an area of over 4000 square kilometres.

Californian firefighters are highly experienced, but this firestorm is like nothing they have seen. Ken Pimlott, director of the California Department of Forestry and Fire Protection, , “The vegetation is so dry, it’s generating so much heat that it’s creating extraordinary conditions.”

, but sometimes it’s too hot even for them. The temperatures generated by some of this year’s fires have been so high that sand on river banks .

This article appeared in print under the headline “California burning”

Huge areas of ocean could suffocate as a result of global warming. But one of these “dead zones” has been shrinking for a century, we now know. Freak local conditions may be at work, but the discovery offers hope that at least one region of the ocean will still be breathable.

Most tropical coastlines have oxygen minimum zones, which form when plankton die, sink and get eaten by bacteria, a process that consumes oxygen. The majority of marine animals cannot breathe in low-oxygen water, and either leave or die.

Around the world, oxygen minimum zones have been growing, partly due to the effects of global warming. But one such zone, in the eastern Pacific off the coast of North and Central America, has been bucking the trend, says of the University of Washington in Seattle.

Using coastal sediments that carry traces of past oxygen levels, Deutsch and his colleagues reconstructed changes in oxygen levels in the eastern tropical Pacific since 1850. They found that the oxygen minimum zone has been shrinking nearly all that time.

Wind churn

That may be the result of changes in the wind. Wind strength is the main factor controlling the size of the dead zone. Powerful winds churn the sea, bringing nutrient-rich water to the surface. This stimulates the growth of plankton and perpetuates the cycle.

The Pacific trade winds weakened for many decades, explaining why the oxygen minimum zone shrank. They have strengthened in recent decades, but forecasts predict they will weaken again as a result of climate change. In the long run, that could mean the oxygen minimum zone keeps on shrinking.

However, that does not mean that other oxygen minimum zones will not grow, says from the National Oceanography Centre in Southampton, UK. He says the Pacific zone is particularly influenced by wind strength, making it unusual.

Journal reference:

Next time you fire up the barbecue, don’t forget the potato salad. It could help counter the effects of all that red meat.

People who eat a lot of red meat have a higher risk of developing colorectal cancer. But previous work has suggested that a type of starch that doesn’t get digested – called resistant starch – can have a protective effect by raising levels of a chemical that dampens some of the genetic changes that precede such cancers.

In the first, small human trial, Karen Humphreys and her colleagues from , Adelaide, Australia, gave 23 healthy volunteers a high red-meat diet for four weeks. They then took cell samples from the volunteers’ guts. These showed an increase in the number of micro RNA molecules – short lengths of genetic material that can silence genes – called miR17-92 and miR21. These elevated micro RNAs are associated with the survival and growth of colorectal cancer cells, and with poorer outcomes for people with that type of cancer.

Next they gave the same volunteers the same diet for another month , but this time supplemented with resistant starch. This is found in foods including cooked potato that has been left to cool, and bananas, though the researchers gave it in the form of a drink.

After this time, cell samples showed that the volunteers’ levels of miR17-92 had, on average, reverted to their original level before the high red-meat diet was introduced. The starch-supplemented diet had no impact on the levels of miR21.

The changes are indicative of much more going on, says Humphreys. “Red meat is likely to be having other cellular effects aside from changing micro RNA levels, such as damage to DNA,” she says, adding that she and her team are now looking at whether resistant starch also moderates other effects.

“Red meat should be eaten in small amounts only and foods that contain fibre or resistant starches should be an important part of the diet,” says , a gastroenterologist at Dundee University, UK.

Journal reference:

(Image: Julian Calder/Getty)

The 8000 strong warriors of the in Xi’an, China, are a formidable enough sight today – but imagine if you could see the whites of their eyes and the blood in their cheeks. When the army was buried 2000 years ago the life-size figurines were painted in a variety of bright hues, including green, blue, pink, red, black, white and lilac. Only traces of that colour remain now, after looting, fire, centuries of water damage and exposure to the open air – all of which took their toll on the paint.

Now we know how these vibrant pigments adhered to the brown clay – animal glue made from ox parts. A team from Northwest University and the Museum of Emperor Qin Shihuang’s Terracotta Army, Xi’an, made the match by comparing the protein molecules in the original paint with artificially aged model samples daubed with different types of binding media.

Now that the paint’s components are better understood, researchers can develop ways to conserve what paint is left, particularly on the thousands of soldiers that still remain to be unearthed.

Journal reference:

This is not a health drink. The waters of North America’s Lake Erie turned lurid green this week, thanks to a bloom of toxic bacteria. The bloom has now receded and the water is drinkable again, but the challenge is to stop it happening again.

The blue-green cyanobacteria built up at the western end of the lake, which is the main source of drinking water for Toledo, Ohio. The bacterium produces a toxin called microcystin, which causes skin rashes, abnormal liver function, diarrhoea, vomiting, numbness and dizziness. Dangerous levels of microcystin forced Toledo to turn off the water supply.

This is not a new problem for Lake Erie. Such blooms were common in the 1960s, mostly because of poor sewage systems dumping phosphorus into the lake. This flow of phosphorus was cut right back in the 1990s, and the ecosystem recovered.

But over the last decade the blooms have become increasingly common again. Phosphorus from fertilisers is running into the water and feeding the bacteria, and invading zebra mussels are eating the bacteria’s competitors.

To prevent blooms, Ohio must stem the flow of phosphorus, says of Ohio State University in Columbus. Farmers should test soil to help them only use as much fertiliser as is necessary, and apply it when planting so unused phosphorus isn’t left lying around.